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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse CD4+ T cells extracted from Egr-2 conditional knock-out mice to gain a new insights about the function of Egr-2

ABSTRACT: This experiment examines the gene expression profiles from CD4+ T cells extracted from Egr-2 conditional knock-out mice (Egr-2 cKO) to gain a new insights about the function of Egr-2

ORGANISM(S): Mus musculus

SUBMITTER: Su-ling Li

PROVIDER: E-MEXP-1698 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Early growth response gene-2 controls IL-17 expression and Th17 differentiation by negatively regulating Batf.

Miao Tizong T Raymond Meera M Bhullar Punamdip P Ghaffari Emma E Symonds Alistair L J AL Meier Ute C UC Giovannoni Gavin G Li Suling S Wang Ping P

Journal of immunology (Baltimore, Md. : 1950) 20121130 1

Early growth response gene (Egr)-2 is important for the maintenance of T cell homeostasis and controls the development of autoimmune disease. However, the underlying mechanisms are unknown. We have now discovered that Egr-2, which is induced by TGF-β and IL-6, negatively regulates the expression of IL-17, but not IL-2 or IFN-γ, in effector T cells. In the absence of Egr-2, CD4 T cells produce high levels of Th17 cytokines, which renders mice susceptible to experimental autoimmune encephalomyelit ...[more]

PMID: 23203924

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Transcription profiling of mouse Egr-1 knock-outs during development (p30 and p42)

Project description:In chicks, the avian homologue of the early growth response protein-1 (ZENK) has been shown to be increased in a special cell type of the retina, the glucagonergic amacrine cells, under conditions that lead to a reduction in eye growth (myopic defocus, recovery of myopia) and decreased under conditions that enhance ocular growth (hyperopic defocus, form-deprivation). The investigation of Egr-1 knock-out mice showed that homozygous knock-out mice with no functional Egr-1 protein developed relative axial myopia at the age of 42 and 56 days, compared to heterozygous- and wildtype Egr-1 knock-out mice. To clarify the role of Egr-1 in the retinal regulation of eye growth, and to get an idea about the biochemical pathways underlying this mechanism, we studied the role of Egr-1 in more detail using Affymetrix microarrays. Experiment Overall Design: Retinal samples of young homozygous Egr-1 knock-out and wildtype mice at the age of 30 days (hm30 and wt30; no difference in axial eye length yet) and 42 days (hm42 and wt42; already a difference in axial eye length of 59 Âµm) were taken to compare the mRNA expression changes over time between these two genotypes and within the same genotype between the two age groups.

2009-12-14 | E-GEOD-16974 | biostudies-arrayexpress

Transcription profiling of human HUVEC cells for Egr-3 knockdown in VEGF-treated cells.

Project description:Analysis of umbilical vein endothelial cells (HUVEC) treated with Egr-3 siRNA under the VEGF treatment for 0,1, and 4 h. Egr-3, a member of early growth response family, is immediately and dramatically induced by VEGF in HUVEC, which regulates expression of many genes related to endothelial activation. Experiment Overall Design: Total 21 samples were derived from triplicate arrays of VEGF-treated si-Control-transfected cells and duplicate arrays of each of the VEGF-treated si-Egr-3-transfected cells.

2009-12-14 | E-GEOD-18913 | biostudies-arrayexpress

Identification of dysregulated transcripts in egr-2(RNAi) planarians

Project description:egr-2 is an injury-responsive gene that is upregulated in the anterior of planarian tail fragments and required for intestinal remodeling. The goal of this study was to identify differentially expressed transcripts in the anterior region of egr-2(RNAi) tail fragments relative to egfp(RNAi) control fragments.

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siRNA-mediated Egr-3 knockdown in VEGF-treated HUVEC

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A profibrotic gene expression program induced by Egr-1 in skin fibroblasts

Project description:Systemic sclerosis (SSc) is characterized by vascular damage, autoimmunity and fibrosis and is associated with highly variable clinical presentation and disease course. Aberrant transforming growth factor-ß (TGF-ß) signaling via the early immediate transcription factor Egr-1 is implicated in the pathogenesis of SSc. To shed light on the role of Egr-1 in fibrosis, regulation of gene expression in human skin fibroblasts overexpressing Egr-1 was examined by genome-wide expression analysis. Over 600 genes were found to be regulated by Egr-1. The Egr-1-responsive gene signature is largely comprised of genes involved in cell proliferation, TGF-ß signaling, wound healing, extracellular matrix synthesis and vascular development. Expression of the Egr-1 responsive genes was evaluated in a microarray dataset comprising skin biopsies from 17 patients with scleroderma and six healthy controls (GEO GSE9285; PMID 18648520). The “Egr-1 responsive gene signature” was enriched in the ‘diffuse-proliferation’ subset of skin biopsies in the patients with diffuse cutaneous SSc (dcSSc), but was not associated with other forms of scleroderma, or with healthy controls. Skin biopsies from patients with scleroderma can provide more insights into the relevant pathological processes in the subset of disease and could be developed into a diagnostic tool for identifying a subset of diffuse scleroderma patients who may be responsive to Egr-1 therapy.

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Egr-1 induced gene expression changes in HUVECs

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Retinal gene expression in Egr-1 knock-out mice during development (p30 and p42)

2009-11-30 | GSE16974 | GEO

A profibrotic gene expression program induced by Egr-1 in skin fibroblasts

2011-10-25 | E-GEOD-27165 | biostudies-arrayexpress

Foxp3 expression is required for the induction of therapeutic tissue tolerance

Project description:CD4+Foxp3+ regulatory T cells (Treg) are essential for immune homeostasis and maintenance of self-tolerance. They are produced in the thymus and also generated de novo in the periphery in a TGFB dependent manner. Foxp3+ Treg are also required to achieve tolerance to transplanted tissues when induced by co-receptor or costimulation blockade. Using TCR transgenic mice to avoid issues of autoimmune pathology we show that Foxp3 expression is necessary and sufficient for tissue tolerance by coreceptor blockade. Moreover, the known need in tolerance induction for TGFB signalling to T cells, can wholly be explained by its role in induction of Foxp3, as such signalling proved dispensable for the suppressive process. We analysed the relative contribution of TGFB and Foxp3 on the transcriptome of TGFB induced Treg. TGFB elicited a large set of downregulated signature genes. The number of genes uniquely modulated due to the influence of Foxp3 alone was surprisingly limited. Retroviral conditional Foxp3 expression proved sufficient to confer transplant-suppressive potency on CD4+ T cells, and was lost once nuclear Foxp3 expression was extinguished. Thus despite the large genetic influence of TGFB exposure on iTreg the crucial Foxp3 influenced signature independent of TGFB is small. These data support a dual role for TGFB and Foxp3 in induced tolerance, where TGFB stimulates Foxp3 expression whose sustained expression is associated with acquisition of tolerance 21 samples were analyzed. 5 replicates of Marilyn.Foxp3hCD2 activated (HY)(Untreated) and TGFB-induced (HYT) cells sorted as CD4+hCD2+ and CD4+hCD2- and 3 replicates of Marilyn.Foxp3-/- activated and TGFβ-experienced (but Foxp3-) cells sorted as CD4+CD2. Pairwise comparisons were generated for the Marilyn Foxp3hCD2 UT versus TGFB induced populations and also for the Marilyn Foxp3-/- UT versus the TGFB experienced cells sorted as CD4+CD2

2012-10-03 | E-GEOD-39529 | biostudies-arrayexpress

Hepatic circadian gene expression in WT and liver specific Egr-1 knockout mice aged 2month, 6month and 12month

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